title: Variance of DDAH/PRMT/ADMA pathway in atrial fibrillation dogs.
abstract: Atrial fibrillation (AF) may cause thrombus formation in the left atrial appendage (LAA). Thrombus formation is associated with LAA endocardial dysfunction. Because asymmetrical dimethylarginine (ADMA) can cause endothelial dysfunction by decreasing nitric oxide (NO) formation, we investigated plasma ADMA and nitrite/nitrate (NO(X)) levels and myocardial dimethylarginine dimethylaminohydrolase-2 (DDAH-2), protein arginine methyltransferase-1 (PRMT-1), and endothelial NO synthase (eNOS) protein contents from AF dogs. The results displayed that plasma ADMA level significantly increased, and plasma NO(X) concentration significantly decreased. Compared with normal heart, DDAH-2 expression was unchanged in the fibrillating atria. However, the DDAH activity was significantly decreased in the fibrillating atria. PRMT-1 expression significantly increased in the LAA and in the left atrium (LA). ENOS expression significantly decreased in the LA. ENOS and PRMT-1 expressions were unchanged in the right atria. Our results suggested that the DDAH-PRMT-ADMA system maybe play a pivotal role in regulating endothelial function in AF.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, PR China.
authors.forename: Hongyan
authors.initials: H
authors.lastname: Liu
authors.forename: Xiufen
authors.initials: X
authors.lastname: Qu
authors.forename: Zhaoguang
authors.initials: Z
authors.lastname: Liang
authors.forename: Weiye
authors.initials: W
authors.lastname: Chen
authors.forename: Wei
authors.initials: W
authors.lastname: Xia
authors.forename: Ying
authors.initials: Y
authors.lastname: Song
mesh_terms: D000581:Amidohydrolases / Q000097:blood / Q000378:metabolism*; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism; D001281:Atrial Fibrillation / Q000097:blood / Q000150:complications / Q000201:enzymology*; D004195:Disease Models, Animal; D004285:Dogs; D015536:Down-Regulation; D004727:Endothelium / Q000201:enzymology; D005260:Female; D008297:Male; D009206:Myocardium / Q000201:enzymology; D009569:Nitric Oxide / Q000097:blood; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism; D011484:Protein-Arginine N-Methyltransferases / Q000097:blood / Q000378:metabolism*; D013927:Thrombosis / Q000201:enzymology* / Q000209:etiology; D015854:Up-Regulation
chemical_list: C487735:dimethylarginine; D009569:Nitric Oxide; D001120:Arginine; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D011484:Protein-Arginine N-Methyltransferases; D000581:Amidohydrolases; C059999:dimethylargininase